Patrice Cacoub1, Pierre Nahon2, Richard Layese3, Lorraine Blaise4, Anne Claire Desbois5, Valérie Bourcier4, Carole Cagnot6, Patrick Marcellin7, Dominique Guyader8, Stanislas Pol9, Dominique Larrey10, Victor De Lédinghen11, Denis Ouzan12, Fabien Zoulim13, Dominique Roulot14, Albert Tran15, Jean-Pierre Bronowicki16, Jean-Pierre Zarski17, Ghassan Riachi18, Paul Calès19, Jean-Marie Péron20, Laurent Alric21, Marc Bourlière22, Philippe Mathurin23, Jean-Frédéric Blanc24, Armand Abergel25, Lawrence Serfaty26, Ariane Mallat27, Jean-Didier Grangé28, Pierre Attali29, Yannick Bacq30, Claire Wartelle31, Thông Dao32, Dominique Thabut33, Christophe Pilette34, Christine Silvain35, Christos Christidis36, Dominique Capron37, Gérard Thiefin38, David Zucman39, Vincent Di Martino40, Corinne Isnard Bagnis41, Marianne Ziol42, Angela Sutton43, Eric Letouze44, Françoise Roudot-Thoraval3, Etienne Audureau3. 1. Sorbonne Universités, UPMC Univ Paris 06, UMR 7211, and Inflammation-Immunopathology-Biotherapy Department (DHU i2B), Paris, France; INSERM, UMR_S 959, Paris, France; CNRS, FRE3632, Paris, France; AP-HP, Groupe Hospitalier Pitié-Salpêtrière, Department of Internal Medicine and Clinical Immunology, Paris, France. Electronic address: patrice.cacoub@aphp.fr. 2. AP-HP, Hôpital Jean Verdier, Service d'Hépatologie, Bondy; Université Paris 13, Sorbonne Paris Cité, "Equipe labellisée Ligue Contre le Cancer", Saint-Denis; Inserm, UMR-1162, "Génomique fonctionnelle des tumeur solides", Paris. 3. AP-HP, Hôpital Henri Mondor, Unité de Recherche Clinique (URC-Mondor), and Université Paris-Est, A-TVB DHU, CEpiA (Clinical Epidemiology and Aging) Unit EA4393, UPEC, Créteil. 4. AP-HP, Hôpital Jean Verdier, Service d'Hépatologie, Bondy. 5. Sorbonne Universités, UPMC Univ Paris 06, UMR 7211, and Inflammation-Immunopathology-Biotherapy Department (DHU i2B), Paris, France; INSERM, UMR_S 959, Paris, France; CNRS, FRE3632, Paris, France; AP-HP, Groupe Hospitalier Pitié-Salpêtrière, Department of Internal Medicine and Clinical Immunology, Paris, France. 6. Unit for Basic and Clinical research on Viral Hepatitis, ANRS (France REcherche Nord & sud Sida-HIV Hépatites-FRENCH). 7. AP-HP, Hôpital Beaujon, Service d'Hépatologie, Clichy. 8. CHU Pontchaillou, Service d'Hépatologie, Rennes. 9. Université Paris Descartes, APHP, Unité d'Hépatologie, Hôpital Cochin, INSERM U-1223 et USM20, Institut Pasteur, Paris, France. 10. Liver Unit and INSERM1183, Montpellier School of Medicine. 11. Hôpital Haut-Lévêque, Service d'Hépatologie, Bordeaux. 12. Institut Arnaud Tzanck, Service d'Hépatologie, St Laurent du Var. 13. Hôpital Hôtel Dieu, Service d'Hépatologie, Lyon. 14. AP-HP, Hôpital Avicenne, Service d'Hépatologie, Bobigny. 15. Institut National de la Santé et de la Recherche Médicale (INSERM), U1065, Team 8, "Hepatic Complications in Obesity", Nice, France and University Hospital of Nice, Digestive Centre, Nice, France. 16. Hôpital Brabois, Service d'Hépatologie, Vandoeuvre-les-Nancy. 17. Service d'Hépato-gastroentérologie, CHU de Grenoble. 18. Hôpital Charles-Nicolle, Service d'Hépato-gastro-entérologie, Rouen. 19. CHU d'Angers, Service d'Hépatologie, Angers. 20. Hôpital Purpan, Service d'Hépatologie, Toulouse. 21. Service de Médecine Interne-Pôle Digestif CHU Toulouse, UMR 152, IRD, Toulouse 3 University. 22. Hôpital Saint Joseph, Service d'Hépatologie, Marseille. 23. Hôpital Claude Huriez, Service d'Hépatologie, Lille. 24. Hôpital St André, Service d'Hépatologie, Bordeaux. 25. Hôpital Hôtel Dieu, Service d'Hépatologie, Clermont-Ferrand. 26. AP-HP, Hôpital Saint-Antoine, Service d'Hépatologie, Paris. 27. AP-HP, Hôpital Henri Mondor, Service d'Hépatologie, Créteil. 28. AP-HP, Hôpital Tenon, Service d'Hépatologie, Paris. 29. AP-HP, Hôpital Paul Brousse, Service d'Hépatologie, Villejuif. 30. Hôpital Trousseau, Unité d'Hépatologie, CHRU de Tours. 31. Hôpital d'Aix-En-Provence, Service d'Hépatologie, Aix-En-Provence. 32. Hôpital de la Côte de Nacre, Service d'Hépatologie, Caen. 33. Sorbonne Universités, UPMC Univ Paris 06, UMR 7211, and Inflammation-Immunopathology-Biotherapy Department (DHU i2B), Paris, France; AP-HP, Groupe Hospitalier de La Pitié-Salpêtrière, Service d'Hépatologie, Paris. 34. CHU Le Mans, Service d'Hépatologie, Le Mans. 35. CHU de Poitiers, Service d'Hépatologie, Poitiers. 36. Institut Mutualiste Montsouris, Service d'Hépatologie, Paris. 37. Hôpital Amiens Nord, Service d'Hépatologie, Amiens. 38. Hôpital Robert Debré, Service d'Hépatologie, Reims. 39. Hôpital Foch, Service d'Hépatologie, Suresnes. 40. Hôpital Jean Minjoz, Service d'Hépatologie, Besançon, France. 41. Sorbonne Universités, UPMC Univ Paris 06, UMR 7211, and Inflammation-Immunopathology-Biotherapy Department (DHU i2B), Paris, France; AP-HP, Groupe Hospitalier Pitié-Salpêtrière, Department of Nephrology, Paris, France. 42. Inserm, UMR-1162, "Génomique fonctionnelle des tumeur solides", Paris; AP-HP, Hôpital Jean Verdier, Service d'Anatomopathologie, Bondy; CRB (liver disease biobank) Groupe Hospitalier Paris Seine-Saint-Denis BB-0033-00027. 43. CRB (liver disease biobank) Groupe Hospitalier Paris Seine-Saint-Denis BB-0033-00027; AP-HP, Hôpital Jean Verdier, Service de Biochimie, Bondy. 44. Inserm, UMR-1162, "Génomique fonctionnelle des tumeur solides", Paris.
Abstract
BACKGROUND: The objective was to examine the role of a sustained virological response (SVR) on major adverse cardiovascular events (MACEs) in patients with compensated hepatitis C virus (HCV) cirrhosis. METHODS: Patients with the following criteria were enrolled in 35 French centers: (1) biopsy-proven HCV cirrhosis; (2) Child-Pugh A; (3) positive viremia; and (4) no prior liver complication, and then prospectively followed. All patients received HCV treatment after inclusion. MACEs included stroke, myocardial infarction, ischemic heart disease, heart failure, peripheral arterial disease, cardiac arrest, and cardiovascular death. SVR, defined as negative viremia 12 weeks posttreatment, was considered as a time-dependent covariate, and its effect on MACE occurrence was assessed. The median follow up was 57.5 months, ending in December 2015. RESULTS: Sixty-two of 878 (7.1%) patients presented a total of 79 MACEs. The main predictive baseline factors of MACEs were Asian ethnic origin, history of MACEs, arterial hypertension, diabetes mellitus, current smoking, low serum albumin level, high total bilirubin level, and low platelet count. In multivariate analysis, SVR was associated with a decreased risk of MACEs (hazard ratio=0.35, 95% CI 0.09-0.97, P=.044), whereas Asian ethnic origin, arterial hypertension, smoking, and low serum albumin level remained predictive of MACE occurrence. The 5-year survival rate was 60.1% versus 87.5% in patients who did versus those who did not present a MACE (P<.001). CONCLUSIONS: In patients with compensated HCV-related cirrhosis, Asian ethnic origin, arterial hypertension, smoking, and low serum albumin are independent predictive factors of cardiovascular events, whereas an SVR is associated with a decreased rate of cardiovascular events.
BACKGROUND: The objective was to examine the role of a sustained virological response (SVR) on major adverse cardiovascular events (MACEs) in patients with compensated hepatitis C virus (HCV) cirrhosis. METHODS:Patients with the following criteria were enrolled in 35 French centers: (1) biopsy-proven HCV cirrhosis; (2) Child-Pugh A; (3) positive viremia; and (4) no prior liver complication, and then prospectively followed. All patients received HCV treatment after inclusion. MACEs included stroke, myocardial infarction, ischemic heart disease, heart failure, peripheral arterial disease, cardiac arrest, and cardiovascular death. SVR, defined as negative viremia 12 weeks posttreatment, was considered as a time-dependent covariate, and its effect on MACE occurrence was assessed. The median follow up was 57.5 months, ending in December 2015. RESULTS: Sixty-two of 878 (7.1%) patients presented a total of 79 MACEs. The main predictive baseline factors of MACEs were Asian ethnic origin, history of MACEs, arterial hypertension, diabetes mellitus, current smoking, low serum albumin level, high total bilirubin level, and low platelet count. In multivariate analysis, SVR was associated with a decreased risk of MACEs (hazard ratio=0.35, 95% CI 0.09-0.97, P=.044), whereas Asian ethnic origin, arterial hypertension, smoking, and low serum albumin level remained predictive of MACE occurrence. The 5-year survival rate was 60.1% versus 87.5% in patients who did versus those who did not present a MACE (P<.001). CONCLUSIONS: In patients with compensated HCV-related cirrhosis, Asian ethnic origin, arterial hypertension, smoking, and low serum albumin are independent predictive factors of cardiovascular events, whereas an SVR is associated with a decreased rate of cardiovascular events.
Authors: Maroussia Roelens; Barbara Bertisch; Darius Moradpour; Andreas Cerny; Nasser Semmo; Patrick Schmid; Beat Müllhaupt; Olivier Clerc; David Semela; Christoph Junker; Francesco Negro; Olivia Keiser Journal: Open Forum Infect Dis Date: 2020-07-25 Impact factor: 3.835
Authors: Fernando Scudiero; Renato Valenti; Rossella Marcucci; Giuseppe D Sanna; Anna Maria Gori; Angela Migliorini; Raffaele Vitale; Betti Giusti; Elena De Vito; Giulia Corda; Rita Paniccia; Davide Zirolia; Mario E Canonico; Guido Parodi Journal: J Am Heart Assoc Date: 2020-09-04 Impact factor: 5.501